Mechanisms of oncogenic stress evolution caused by obesity

利用活体小鼠体内p16INK4a和p16INK4a表达的生物发光成像系统，我们发现，肥胖和p53失活等致癌因素可以抑制脂肪组织前体细胞中p16INK4a的表达。P53的失活增加了脂肪组织前体细胞的DNA损伤和活性氧物种(ROS)，表明肥胖会在这些细胞中产生致癌压力。

Using a bioluminescence imaging system for p16^<INK4a> expression in living mice, we show that oncogenic insults such as obesity and p53 inactivation provoke de-repression of p16INK4a expression in progenitors of adipose tissue. p53 inactivation increases DNA damage and reactive oxygen species(ROS) in progenitors of adipose tissues, indicating that obesity generates oncogenic stress in these cells.